The clinical course of patients with Bell's palsy varies from rapid early complete recovery to a more debilitating course of permanent disfiguring facial nerve dysfunction. Fortunately, most Bell's palsies recover completely and spontaneously, with 85% of patients with Bell's palsies having a full or near full recovery. Those patients who have a complete paralysis persisting for 8 weeks are likely to develop sequelae. All patients, however, regain some function within 6 months and, if no motion returns, a vigorous search for another origin should begin.
The pathogenesis of Bell's palsy is obscure. Histologic and clinical data exist to establish that injury to the nerve and loss of impulse conduction result from edema and constriction in an unexpandable bony canal. Prolonged or increased constriction leads to Wallerian degeneration. Viral etiology has been proposed as a cause for Bell's palsy. In 1975, Adour et al.4 found elevated viral antibody titers in 40 patients with Bell's palsy and deduced that reactivated herpes simplex virus (HSV) was the probable cause of Bell's palsy. Subsequent information has also added to the validity that viral etiology is a cause of Bell's palsy. Animal studies have shown that herpes virus inoculation can produce facial paralysis in animals.5 Other studies have shown viral DNA in endoneural fluid and muscle in patients with Bell's palsy and HSV.
The use of corticosteroids to treat the patients with Bell's palsy has been widely accepted.6 Several studies show more favorable outcome with steroid therapy. It may reduce the risk of denervation if initiated early on. It may prevent synkinesis and progression of incomplete to complete paralysis; it may also hasten recovery. Patients presenting within the first week of facial paralysis are administered corticosteroid therapy consisting of prednisone, 1 mg/kg over three equal divided doses for the first week. Patients are then reevaluated during the second week after onset of facial paralysis. If their symptoms are resolving, the prednisone is tapered over the following week. The side effects of steroids are well documented, including hyperglycemia, emotional changes, fluid and electrolyte disturbances, gastrointestinal tract hemorrhage, and aseptic necrosis of the hip.
Adour et al.7 examined the empirical use of acyclovir and steroids for patients with Bell's palsy. This double-blind study compared 99 patients with Bell's palsy who were treated with either acyclovir-prednisone or placebo-prednisone. The outcome in the acyclovir-prednisone-treated patients was superior to that of patients who received placebo-prednisone. Dosages of acyclovir were administered at 400 mg 5 times daily.
Surgical decompression of the facial nerve remains a controversial and emotional subject. Historically, the vertical and horizontal segments of the facial nerve in the mastoid were recommended for decompression. The preferred route was a trans-mastoid approach. Little if any therapeutic effect was observed in the ultimate outcome of patients with acute facial paralysis after decompression.
Anatomic and electrophysiologic evidence of a specific anatomic site of lesion in Bell's palsy emerged focusing on the meatal segment of the facial nerve. Both transmastoid and mid dle fossa approaches have been advocated to gain access to this region. The transmastoid approach to the geniculate ganglion and labyrinthine segment avoids a craniotomy. It does require the removal of the incus in poorly pneumatized mastoids. In our opinion, it is impossible to achieve adequate exposure of the labyrinthine segment consistently because the ampulated end of the superior canal prevents complete exposure of the proximal labyrinthine segment. May8 used the transmastoid approach for facial nerve decompression and found decompression to improve recovery in patients whose maximal nerve stimulation responses were reduced by 75% or more. However, long-term follow-up evaluation of these patients failed to show any significant benefit as compared with patients who didn't have surgery, and was ultimately abandoned.
The meatal foramen is most adequately approached by the middle cranial fossa.9 Fisch9 performed decompression of the facial nerve in Bell's palsy via the middle fossa approach when ENOG was less than 10% of the normal side. All patients who underwent decompression demonstrated satisfactory return of facial function. The 90% of satisfactory outcome with surgery compared favorably with a 50% chance of satisfactory turn noted in unoperated patients matched by EMG profile.
Surgery performed on eight patients during the third week after the onset of palsy, when degeneration exceeded 90%, did not significantly improve the return of facial function. However, two patients in this group demonstrated exceptional return of facial motion after decompression. Although this experience suggests that middle fossa craniotomy for decompression ofthe meatal portion of the facial nerve may have some beneficial affects in reducing the sequelae of Bell's palsy, it is only suggestive. Further studies are needed and are being performed. Because these studies are not completed, we have used medical therapy consisting of, prednisone-acyclovir as our mainstay of treatment of Bell's palsy. We have reserved middle fossa craniotomy decompression of the facial nerve for the patient at high risk of sequelae, and only after the patient has been informed of possible risks and complications of the procedure.
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